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MNT, MAX Dimerization Protein Proteins (MNT)

The Myc/Max/Mad network comprises a group of transcription factors that co-interact to regulate gene-specific transcriptional activation or repression. Additionally we are shipping MNT Antibodies (25) and and many more products for this protein.

list all proteins Gene Name GeneID UniProt
MNT 17428 O08789
MNT 4335 Q99583
Rat MNT MNT 287521  
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Top MNT Proteins at antibodies-online.com

Showing 3 out of 3 products:

Catalog No. Origin Source Conjugate Images Quantity Supplier Delivery Price Details
HOST_Escherichia coli (E. coli) Human His tag „Crystallography Grade“ protein due to multi-step, protein-specific purification process 1 mg Log in to see 29 to 34 Days
$4,331.68
Details
HOST_Escherichia coli (E. coli) Mouse His tag „Crystallography Grade“ protein due to multi-step, protein-specific purification process 1 mg Log in to see 29 to 34 Days
$4,331.68
Details
HOST_Wheat germ Human GST tag 10 μg Log in to see 9 Days
$405.71
Details

MNT Proteins by Origin and Source

Origin Expressed in Conjugate
Mouse (Murine)

Human ,
,

More Proteins for MNT, MAX Dimerization Protein (MNT) Interaction Partners

Mouse (Murine) MNT, MAX Dimerization Protein (MNT) interaction partners

  1. results redefine the physiological relationship between Mnt and Myc (show MYC Proteins) and requirements for Myc (show MYC Proteins)-driven oncogenesis

  2. Mxd4 (show MXD4 Proteins) and Mnt upregulation following OX40 (show TNFRSF4 Proteins) engagement most likely increases T-cell survival

  3. There is a unique negative regulatory role for Mnt in governing key Myc (show MYC Proteins) functions associated with cell proliferation and tumorigenesis.

  4. Mnt may serve a general role as a Myc (show MYC Proteins) antagonist.[Review]

  5. Mnt represses Myc target genes and Myc functions as an oncogene by relieving Mnt-mediated repression

  6. Loss of protein Mnt in mice results in decreased viability, defective embryonic growth and craniofacial defects.

  7. These results demonstrate that Mnt-Myc (show MYC Proteins) antagonism plays a fundamental role in regulating cell cycle entry and proliferation.

  8. Mnt is expressed both in growth-arrested and proliferating mouse fibroblasts and is phosphorylated when resting cells are induced to re-enter the cell cycle

  9. Mnt functions as a tumor suppressor and reveal a critical and surprising role for Mnt in the regulation of T-cell development and in T-cell-dependent immune homeostasis.

  10. The switch from Mnt-Max to Myc (show MYC Proteins)-Max during bile duct ligation (cholestasis) and in hepatocytes treated with lithocholic acid is responsible for the induction in p53 (show TP53 Proteins) and cyclin D1 (show CCND1 Proteins) expression and contributes to apoptosis.

Human MNT, MAX Dimerization Protein (MNT) interaction partners

  1. Here we review the activities of MYC (show MYC Proteins), MNT and other MAX interacting proteins in the setting of T and B cell activation (show BLNK Proteins) and oncogenesis

  2. The data demonstrate that the balance between c-Myc and Mnt activity determines the transcriptional outcome of the hTERT promoter by modulation of the chromatin architecture.

  3. The results suggest that MNT, via interaction with Nck1 (show NCK1 Proteins), inhibits hepatoma cell migration.

  4. downregulation MYCN was reflected in a decreased MYCN/Max DNA-binding activity while the Mnt/Max binding did not change during differentiation

  5. Serum stimulation of quiescent cells results in phosphorylation of Mnt and disruption of the critical Mnt-mSin3-HDAC1 (show HDAC1 Proteins) interaction. This in turn leads to increased expression of the Myc (show MYC Proteins)/Mnt target gene cyclin D2 (show CCND2 Proteins). Review.

  6. Mad1, Mxi1 and Rox genes were expressed and displayed mutations in haematological malignancies.

  7. Mxd1 (show MXD1 Proteins) D112a and Max N78a and H81d, which are located in the leucine zippers of the proteins, can dictate the specificity of heterodimerization and whether or not the Mxd1 (show MXD1 Proteins)/Max/DNA complex forms.

  8. Missense mutations in Mad1, Mxi1 and Rox were found in acute leukemia patients.

  9. The switch from Mnt-Max to Myc (show MYC Proteins)-Max during bile duct ligation (cholestasis) and in hepatocytes treated with lithocholic acid is responsible for the induction in p53 (show TP53 Proteins) and cyclin D1 (show CCND1 Proteins) expression and contributes to apoptosis.

MNT Protein Profile

Protein Summary

The Myc/Max/Mad network comprises a group of transcription factors that co-interact to regulate gene-specific transcriptional activation or repression. This gene encodes a protein member of the Myc/Max/Mad network. This protein has a basic-Helix-Loop-Helix-zipper domain (bHLHzip) with which it binds the canonical DNA sequence CANNTG, known as the E box, following heterodimerization with Max proteins. This protein is likely a transcriptional repressor and an antagonist of Myc-dependent transcriptional activation and cell growth. This protein represses transcription by binding to DNA binding proteins at its N-terminal Sin3-interaction domain.

Gene names and symbols associated with MNT

  • MAX binding protein (MNT)
  • max binding protein (Mnt)
  • MNT, MAX dimerization protein (MNT)
  • MNT, MAX dimerization protein (Mnt)
  • MNT, MAX dimerization protein (mnt)
  • bHLHd3 protein
  • MAD6 protein
  • MGC98824 protein
  • mnt protein
  • MXD6 protein
  • rox protein

Protein level used designations for MNT

max-binding protein MNT , myc antagonist MNT , MAX binding protein , Max-interacting protein , class D basic helix-loop-helix protein 3 , max binding protein

GENE ID SPECIES
491202 Canis lupus familiaris
618576 Bos taurus
17428 Mus musculus
4335 Homo sapiens
287521 Rattus norvegicus
734360 Xenopus laevis
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